Índice de resistividade renal como preditor da revascularização renal para hipertensão renovascular / Renal resistance index predicting outcome of renal revascularization for renovascular hypertension

FUNDAMENTO: A estenose arterial renal (EAR) é uma causa potencialmente reversível de hipertensão arterial sistêmica (HAS) e nefropatia isquêmica. Apesar da revascularização bem sucedida, nem todos os pacientes (pt) apresentam melhora clínica e alguns podem piorar. OBJETIVO: O presente estudo se destina a avaliar o valor do índice de resistividade renal (IR) como preditor dos efeitos da revascularização renal. MÉTODOS: Entre janeiro de 1998 e fevereiro de 2001, 2.933 pacientes foram submetidos ao duplex ultrassom renal. 106 desses pacientes apresentaram EAR significativa e foram submetidos a angiografia e revascularização renal. A pressão arterial (PA) foi medida antes e depois da intervenção, em intervalos de até 2 anos e as medicações prescritas foram registradas. Antes da revascularização, o IR foi medido em 3 locais do rim, sendo obtida uma média dessas medições. RESULTADOS: Dos 106 pacientes, 81 tiveram IR<80 e 25 RI>80. A EAR foi corrigida somente por angioplastia (PTA) em 25 pts, PTA + stent em 56 pts e cirurgicamente em 25 pts. Dos pacientes que se beneficiaram da revascularização renal; 57 dos 81 pacientes com IR <80 apresentaram melhora em comparação a 5 de 25 com IR > 80. Usando um modelo de regressão logística múltipla, o IR esteve significativamente associado à evolução da PA (p = 0,001), ajustado de acordo com os efeitos da idade, sexo, PAS, PAD, duração da hipertensão, o tipo de revascularização, número de fármacos em uso, nível de creatinina, presença de diabete melito, hipercolesterolemia, volume sistólico, doença arterial periférica e coronariana e tamanho renal (OR 99,6-95 por centoCI para OR 6,1-1.621,2). CONCLUSÃO: A resistividade intrarrenal arterial, medida por duplex ultrassom, desempenha um papel importante na predição dos efeitos pós revascularização renal para EAR.

BACKGROUND: Renal artery stenosis (RAS) is a potentially correctable cause of hypertension and ischemic nephropathy. Despite successful renal revascularization, not all patients (pt) overcome it and some get worse. OBJECTIVE: This study was designed to assess the value of renal resistance index (RI) in predicting the outcome of renal revascularization. METHODS: Between Jan 1998 and Feb 2001, 2,933 pts were referred to renal duplex ultrasound. 106 out of these had significant RAS and underwent angiography and renal revascularization. Arterial blood pressure (BP) was measured before and after the intervention, at intervals of up to 2 years and medications recorded. Prior to revascularization, RI was measured at 3 sites of each kidney and averaged. RESULTS: Out of the 106 patients, 81 had RI<80 and 25 RI>80. RAS was corrected with angioplasty (PTA) alone in 25 pts, PTA + stent in 56 pts and corrected by surgery in 25 pts. Of patients who benefited from renal revascularization; 57 of the 81 patients with RI <80 improved as compared to 5 of 25 with RI>80. Using a multiple logistic regression model, RI was significantly associated with BP outcome (p=0.001), adjusted for the effects of age, sex, SBP, DBP, duration of hypertension, type of revascularization, number of medication in use, creatinine level, presence of diabetes mellitus, hypercholesterolemia, stroke, peripheral and coronary artery disease and kidney size (OR 99.6 - 95 percentCI for OR 6.1 to 1,621.2). CONCLUSION: Intrarenal arterial resistance measured by duplex ultrasound plays an important role in predicting BP outcome after renal revascularization for RAS.

High susceptibility of activated lymphocytes to oxidative stress-induced cell death

The present study provides evidence that activated spleen lymphocytes from Walker 256 tumor bearing rats are more susceptible than controls to tert-butyl hydroperoxide (t-BOOH)-induced necrotic cell death in vitro. The iron chelator and antioxidant deferoxamine, the intracellular Ca2+ chelator BAPTA, the L-type Ca2+ channel antagonist nifedipine or the mitochondrial permeability transition inhibitor cyclosporin A, but not the calcineurin inhibitor FK-506, render control and activated lymphocytes equally resistant to the toxic effects of t-BOOH. Incubation of activated lymphocytes in the presence of t-BOOH resulted in a cyclosporin A-sensitive decrease in mitochondrial membrane potential. These results indicate that the higher cytosolic Ca2+ level in activated lymphocytes increases their susceptibility to oxidative stress-induced cell death in a mechanism involving the participation of mitochondrial permeability transition.

O presente estudo demonstra que linfócitos ativados de baço de ratos portadores do tumor de Walker 256 são mais susceptíveis à morte celular necrótica induzida por tert-butil hidroperóxido (t-BOOH) in vitro quando comparados aos controles. O quelante de ferro e antioxidante deferoxamina, o quelante intracelular de Ca2+ BAPTA, o antagonista de canal de Ca2+ nifedipina ou o inibidor da transição de permeabilidade mitocondrial ciclosporina-A, mas não o inibidor de calcineurina FK-506, inibiram de maneira similar a morte celular induzida por t-BOOH em linfócitos ativados e controles. Os linfócitos ativados apresentaram redução do potencial de membrana mitocondrial induzida por t-BOOH num mecanismo sensível a ciclosporina-A. Nossos resultados indicam que o aumento da concentração de Ca2+ citosólico em linfócitos ativados aumenta a susceptibilidade dos mesmos à morte celular induzida por estresse oxidativo, num mecanismo envolvendo a participação do poro de transição de permeabilidade mitocondrial.

Pathogenesis of hepatic encephalopathy: update on molecular mechanisms.

Hepatic encephalopathy (HE) is a major neuropsychiatric complication of acute and chronic liver failure. Neuropathologically, HE in chronic liver failure is characterized by astrocytic (rather than neuronal) changes known as Alzheimer type II astrocytosis and in altered expression of key astrocytic proteins. Magnetic resonance imaging in cirrhotic patients reveals bilateral signal hyperintensities in globus pallidus on T1-weighted imaging, which appear to result from manganese deposition. Proton (1H) magnetic resonance spectroscopy shows an increase in glutamine resonance in brain, a finding that confirms previous biochemical studies and is consistent with increased uptake of ammonia by the brain (glutamine synthesis). Recent molecular biological studies show an increased expression of several genes coding for neurotransmitter-related proteins in chronic liver failure. Such genes include those for monoamine oxidase (MAO-A isoform), nitric oxide synthase (nNOS isoform) and the peripheral-type benzodiazepine receptor. Activation of these systems may lead to alterations of monoamine and amino acid neurotransmitter function and changes in cerebral blood flow in chronic liver failure.

Introduction de la peste porcine africaine à Madagascar : histoire et leçons d'une émergence

La Peste Porcine Africaine (PPA) a récemment fait son apparition à Madagascar.Officiellement diagnostiquée fin 1998, la PPA a vraisemblablement été introduite à Madagascar en 1997 dans le sud du pays à partir de virus provenant du continent africain. La PPA s'estensuite propagée dans la quasi-totalité du pays à l'exception de la région d'Antsiranana (Nord) et de Morondava (Ouest). La maladie a eu des conséquences économiques désastreuses et aentraîné la désorganisation de la filière porcine malgache.Nous rapportons ici l'histoire de cette émergence et l'existence de particularités locales comme la présence de vecteurs, les tiques du genre Ornithodoros - O. moubata porcinus - et de réservoirs sauvages potentiels comme le potamochère - Potamochoerus larvatus - qui compromettentl'éradication de la maladie.Ces faits renforcent la nécessité pour Madagascar de disposer d'un système d'alerte et de riposte rapide

Mitochondrial oxidative damage promoted by a synergism betweem Ca2+ and prooxidants: inner membrane permeabilization and mtDNA breakage

Oxidative damage of mitochondria induced by a synergism between Ca2+ and prooxidants is mediated by the attack of mitochondria-generated reactive oxygen species to membrane proteins, lipids and DNA. This results in mitochondrial DNA fragmentation, lipid peroxidation and oxidation of vicinal protein thiols producing high molecular weight membrane protein aggregates. The membrane protein alterations lead to a condition called mitochondrial membrane permeability transition, characterized by formation of nonspecific membrane protein pores sensitive to cyclosporin A, EGTA, dithiothreitol, Mg2+ and ADP. We propose that these alterations are related to the mechanisms by which cells are killed by a series of toxins, xenobiotics or pathological conditions such as prolonged hypoxia or ischemia/reperfusion.

Ulcera de córnea infecciosa em ceratoplastia penetrante / Infections corneal ulcer in penetrating keratoplasty

Dos 181 casos de úlcera de córnea admitidos ao Kellogg Eye Center entre 1975 e 1983, 26 ocorreram em olhos que haviam sido submemtidos a ceratoplastia penetrante. Ceratopatia bolhosa foi a indicaçäo mais freqüente para ceratoplastia penetrante. O intervalo médio de tempo entre a ceratoplastia e o início da ulceraçäo foi de 7 meses